Oxidative stress arises from an imbalance between pro-oxidant and antioxidant levels, where the pro-oxidant status, primarily reactive oxygen species (ROS), exceeds the antioxidant defense. This imbalance can damage cellular components such as membranes, lipids, proteins, DNA, and lipoproteins, leading to various chronic and degenerative diseases. The human body defends against oxidative stress through antioxidant mechanisms. Numerous studies have shown that physical exercise increases ROS production, mainly through enhanced activity of phospholipase A2 (PLA2), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and xanthine oxidase (XO). If ROS accumulates excessively, it can result in oxidative stress. During anaerobic exercise, lipid peroxidation levels can rise significantly for up to 48 hours post-exercise. The primary sources of free radical production during exercise include the mitochondrial electron transport chain, ischemia-reperfusion injury, and local inflammation, all of which induce oxidative stress.
Acute changes in oxidative stress biomarkers after exercise are often accompanied by an increase in antioxidant response. For instance, levels of uric acid (UA), catalase (CAT), and glutathione peroxidase (GPX) increase after 10 minutes to 4-8 hours of anaerobic exercise. Various types of exercise also stimulate mitochondrial biogenesis, though it remains unclear whether anaerobic or aerobic exercise is more effective in promoting this process in humans. Mitochondria, critical for cellular energy production, generate energy by transferring electrons from food into the respiratory chain system, involving various complex proteins. High-intensity interval training (HIIT) in aerobic exercises like cycling and walking prompts cells to produce more proteins for mitochondria and their ribosomes, effectively counteracting cellular aging. Endurance exercise (low to moderate intensity for 30 to 60 minutes) is well-known to enhance mitochondrial function in skeletal muscle, though the effects of anaerobic exercise on mitochondrial biogenesis are less studied.
Both aerobic and anaerobic exercises positively affect lipid metabolism. Aerobic exercise is particularly effective in improving lipid profiles, notably increasing high-density lipoprotein (HDL). An Australian study showed that aerobic exercise significantly reduced total cholesterol, low-density lipoprotein (LDL), and triglycerides (TG), while increasing HDL by about 0.05 mmol/L. A meta-analysis by Kelley et al. concluded that aerobic exercise increases HDL by 9% and reduces TG by 11%, though it does not significantly alter total cholesterol or LDL levels. Anaerobic exercise has also shown positive effects on lipid profiles. A European study on 16 obese subjects found that combined aerobic and anaerobic training led to a greater reduction in non-esterified fatty acids and body mass index than aerobic training alone.
In summary, physical exercise impacts oxidative stress, mitochondrial function, and metabolic parameters, yet the distinct effects of aerobic versus anaerobic exercise on these factors remain unclear. Aerobic and anaerobic exercises differ primarily in their oxygen (O2) requirements. Aerobic exercises, such as long-distance running, cycling, and jogging, are performed at low to moderate intensity (40% to 70% of VO2max) and rely on oxygen for sustained periods. Anaerobic exercise is performed at high intensity (75% to 100% of VO2 max) and does not rely on oxygen (O2) supply. Examples include sprints of 100 meters or less, throwing sports, and similar activities.
